title: Localization of culprit lesions in coronary arteries of patients with ST-segment elevation myocardial infarctions: relation to bifurcations and curvatures.
abstract: BACKGROUND
  Although culprit lesions in ST-segment elevation myocardial infarction (STEMI) cluster in the proximal coronary arteries, their relationship to bifurcations and curvatures, where blood flow is disturbed, is unknown. We hypothesized that (a) culprit lesions localize to disturbed flow distal to bifurcations and curvatures and (b) the distribution of culprit lesions in the left (LCA) and right coronary arteries (RCA) and resulting infarct size are related to the location of bifurcations and curvatures.
  
  
  METHODS
  Emory University's contribution to the National Cardiovascular Data Registry was queried for STEMIs. Using quantitative coronary angiography, the distances from the vessel ostium, major bifurcations, and major curvatures to the culprit lesion were measured in 385 patients.
  
  
  RESULTS
  Culprit lesions were located within 20 mm of a bifurcation in 79% of patients and closer to the bifurcation in the LCA compared with the RCA (7.4 ± 7.3 vs 17.7 ± 14.8 mm, P < .0001). Of RCA culprit lesions, 45% were located within 20 mm of a major curvature. Compared with those in the RCA, culprit lesions in the LCA were located more proximally (24.4 ± 16.5 vs 44.7 ± 28.8 mm, P = .0003) and were associated with larger myocardial infarctions as assessed by peak creatine kinase-MB (208 ± 222 vs 140 ± 153 ng/dL, P = .001) and troponin I (59 ± 62 vs 40 ± 35 ng/dL, P = .0006) and with higher in-hospital mortality (5.2% vs 1.1%, P = .04).
  
  
  CONCLUSIONS
  In patients with STEMI, culprit lesions are frequently located immediately distal to bifurcations and in proximity to major curvatures where disturbed flow is known to occur. This supports the role of wall shear stress in the pathogenesis of STEMI.
authors.affiliation: Emory University School of Medicine, Atlanta, GA, USA.
authors.forename: Michael C
authors.initials: MC
authors.lastname: McDaniel
authors.forename: Erin M
authors.initials: EM
authors.lastname: Galbraith
authors.forename: Ahmad M
authors.initials: AM
authors.lastname: Jeroudi
authors.forename: Omar R
authors.initials: OR
authors.lastname: Kashlan
authors.forename: Parham
authors.initials: P
authors.lastname: Eshtehardi
authors.forename: Jin
authors.initials: J
authors.lastname: Suo
authors.forename: Saurabh
authors.initials: S
authors.lastname: Dhawan
authors.forename: Michele
authors.initials: M
authors.lastname: Voeltz
authors.forename: Chandan
authors.initials: C
authors.lastname: Devireddy
authors.forename: John
authors.initials: J
authors.lastname: Oshinski
authors.forename: David G
authors.initials: DG
authors.lastname: Harrison
authors.forename: Don P
authors.initials: DP
authors.lastname: Giddens
authors.forename: Habib
authors.initials: H
authors.lastname: Samady
mesh_terms: D054058:Acute Coronary Syndrome / Q000473:pathology; D000368:Aged; D017023:Coronary Angiography; D003331:Coronary Vessels / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging* / Q000473:pathology* / Q000503:physiopathology; D058226:Plaque, Atherosclerotic / Q000473:pathology* / Q000503:physiopathology; D012039:Regional Blood Flow